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Contact us at firstname.lastname@example.org 22 Macular Edema and Cataract Surgery Miltiadis K Tsilimbaris, Chrysanthi Tsika, Vasilios Diakonis, Aleksandra Karavitaki and Ioannis Pallikaris University of Crete Medical School, Department of Ophthalmology Greece
1. Introduction Macular edema (macular oedema) is the accumulation of fluid within the retinal spaces, among the several layers of the tissue due to mechanical factors (anatomic failure, traction) or chemical factors (inflammation, drugs). The macular edema causes thickening of the retina and it may be diffuse or local. Cystoid macular edema (CME) also spelled as cystoid macular oedema (CMO) is the local form of the condition when it accumulates into cystic spaces mainly in the outer layers of the central retina (macula). CME is a painless condition.
The effect on visual function depends on the severity of the condition and is usually associated with blurred or distorted vision. CME can be recognized by visual acuity reduction, characteristic appearance of the macula during fundoscopy, fluorescein angiography or ocular coherence tomography (OCT). It is important to distinguish the different varieties of CME that can range from fluorescein angiography findings only (angiographic CME) to symptomatic CME. Chronic cystoid macular edema refers to clinically significant CME that persist for more than six months (Gass & Norton, 1969;
Berkow et al., 1997).
The cause of CME depends on the underlying disease process. It has been reported in association with local ocular conditions (epiretinal membrane, subretinal neovascularization), ocular or systemic vascular diseases (central and branch retinal vein obstruction, diabetic retinopathy), inflammatory conditions (pars planitis), conditions that lead to mechanical/tractional stress of the retina (vitreomacular traction syndrome), use of medications (epinephrine, latanoprost), and inherited diseases (retinitis pigmentosa). Rare causes of CME such as juvenile retinoschisis, Goldmann-Favre disease and nicotinic acid maculopathy are characterized by different pathogenesis, positive family history and different patterns in the fluorescein angiography.
Postoperative CME represents a well-known distinct entity associated with a variety of intraocular operations. Operations such as scleral buckling, pneumatic retinopexy or combined PKP and transscleral sutured posterior chamber IOL implantation can be complicated by postoperative CME (Notage et al., 2009; Van der Schaft et al, Tunc et al., 2007). CME following cataract surgery is currently the most commonly encountered postoperative CME. Post-cataract or Pseudophakic CME was initially described by Irvine SR in 1953 and Gass & Norton in 1966; this is why this entity is also known as Irvine-Gass syndrome (Irvine, 1953, 1976; Gass & Norton, 1966). Although most patients with CME after cataract surgery are visually asymptomatic, demonstrating only CME findings on 324 Cataract Surgery angiography and on OCT, clinically significant CME still occurs even after an uncomplicated cataract extraction using phacoemulsification.
2. Incidence, epidemiology, risk factors CME is the most common cause for sub-optimal visual outcome after cataract extraction procedures and represents today the most common cause of unexpected visual loss after uneventful cataract surgery (Ray & D’Amico, 2002). CME may occur after both complicated and uncomplicated cataract surgery, with no significant gender or race predilection.
Angiographic CME is detected in fluorescein angiography as a capillary perifoveal leakage with a petaloid appearance while in clinical CME biomicroscopic findings together with significant visual impairment are also present. Older reports on angiographic CME after intracapsular cataract extraction (ICCE) mention rates as high as 50-70% while after extracapsular cataract extraction (ECCE) the rate has been reported to be close to 18% ranging from 16 to 40% (Ray & D’Amico, 2002, Nagpal et al., 2001). Ursell et al. (1999) investigated the existence of angiographic CME after phacoemulsification the 60th day after surgery; they reported 19% of angiographic CME in 103 eyes, with no development of clinical CME in any of these eyes.
The incidence of clinically significant CME has been reported to be from 1% to 12% depending on factors such as surgical technique, selection of IOL, intra-operative complications and post-operative management. In 1998, Flach performed fluorescein angiograms in all cases with VA lower than 20/40 after ECCE with PC-IOL implantation and revealed a 7% incidence of post-operative clinical CME. The lack of use of postoperative steroids may have contributed to that high rate in this particular study. Following an uncomplicated phacoemulsification with an intact posterior capsule, the rate for CME has been reported to be as low as 0-2%. (Mentes et al., 2003; Flach et al., 1998). Recently, Loewenstein & Zur (2010) reported a rate of 0.1-2.35% for clinical CME following modern cataract surgery techniques.
Risk factors responsible for the development of CME after cataract extraction include several intraoperative complications such as posterior capsular rupture, vitreous loss and vitreous incarceration into the incision site and anterior chamber. Advanced age has been also reported as a risk factor for the development of the syndrome (Rossetti & Autelitano, 2000).
Percival (1998) studied the effect of different factors on CME development after lens implantation. He reported a 13% incidence of CME after ECCE with intact posterior capsule, while if the capsule was ruptured the rate increased to 27%. Moreover, vitreous in the anterior chamber resulted in the appearance of CME in 33% of cases. Other authors have also shown the relationship between posterior capsule rapture and postoperative CME (Nikica et al., 1992; Chambless et al., 1979). The same positive correlation with postoperative CME has been reported by several authors for vitreous loss (Ah-Fat et al., 1998; Iwao et al., 2008). In a 2000 review by Rosetti & Autelitano, vitreous loss was correlated with an overall increase in CME by 10-20%. The use of iris supported IOLs is also associated with increased incidence and late onset of CME, which has been attributed to the chronic irritation of the iris. Iris is a tissue that responds to injury with secretion of inflammatory mediators.
Gulkilik et al. (2006) found the presence of CME in 70% of patients after iris trauma compared to 20,5% of patients without iris injury. In general, the incidence of CME in complicated cases of cataract extraction has been reported to range from 1.5% to 35.7% 325 Macular Edema and Cataract Surgery (Nikica et al. 1992). The type of intraocular lens (IOL) implanted may also play some role in postoperative CME formation. Kraff et al. (1985) reported that the use of ultraviolet (UV)filtering IOLs might reduce the formation of angiographic CME. Finally, Ferrrari et al. (1999) reported an association between macular edema formation and the amount of energy during phacoemulsification; in their study, a higher incidence of CME was associated with energies that exceeded one joule. On the other hand several other factors do not seem to play any significant role. In a study performed by Gulkilik et al (2006) no correlation was found between postoperative CME and cataract type, iris colour or pseudoexfoliation; in the same study no correlation between phacoemulsification time and CME development was found.
The risk of visually significant CME has decreased with the development of advanced surgical techniques, such as modern phacoemulsification with micro-incisional techniques and foldable intraocular lenses (IOLs), when compared to older techniques, especially intracapsular cataract extraction (Wetzig et al, 1979; Sorr et al, 1979). If the diagnosis of visually significant ME is based on visual loss to the 20/40 level or worse, the incidence is 2 - 10% following ECCE or ICCE and 0 - 2% following phacoemulsification with an intact posterior capsule. However, in at least one large series comparing postoperative CME after ECCE and phacoemulsification in patients with no underlying systemic disease, no significant differences were found between the two techniques. Even though the angiographic CME was slightly higher for ECCE, the clinical incidence was similar (0-6% for phacoemulsification compared to 0-7.6% for ECCE) (Powe et al., 1994).
The risk of CME formation after cataract surgery may increase in the presence of several ocular or systemic diseases when compared with history free patients. In a review study by Rotsos et al it was suggested that cataract surgery in diabetic patients might accelerate preexisting diabetic macular edema leading to poor visual outcome. Even in the absence of diabetic macular edema, diabetic patients tend to have a higher risk of developing CME after uncomplicated cataract extraction (Dowler et al., 1995, 2000; Dowler & Hykin, 2001;
Schatz, 1994; Pollack, 1992). In addition to diabetes, uveitis is also a significant pre-operative condition predisposing to CME. The rates reported in the literature may reach 56% while in most case it is recurrent (Krishna et al., 1998; Estafanous et al., 2001).). For this reason a careful selection of patients with uveitis has been suggested as a way to decrease the frequency of postoperative CME development (Suresh et al., 2001). Preoperative steroids may be given, topically and/or systemically in uveitis patients. The presence of epiretinal membrane also predisposes to increase of macular thickness and macular edema after cataract extraction. Finally, patients under local therapy with prostaglandin analogues have been reported to have a higher incidence of CME after cataract extraction. Agange et al presented a case report of a glaucomatic patient who developed recurrent CME with three separate trials of three different prostaglandins after uncomplicated cataract surgery. Other studies have also reported same findings (Yeh & Ramanathan, 2002; Altintaş et al., 2005;
Panteleontidis et al., 2010).
In a study conducted in our institution, we prospectively examined macular thickness alterations after uncomplicated phacoemulsification in four different groups of patients.
One group consisted of otherwise fit patients while the others included patients with diabetes, epiretinal membrane and glaucoma. We concluded that regardless of group, a statistically significant mean foveal thickness (MFT) increase occurs one month after surgery, while this increase regresses six months after surgery. Even though MFT regressed during the follow up period, in patients with diabetes mellitus and epiretinal membrane it 326 Cataract Surgery remained significantly higher even six months after cataract surgery. With regard to diabetic patients, these showed the greatest difference between postoperative and preoperative macular thickness, indicating that the underlying pathophysiology is influenced significantly by the cataract extraction process. Despite these macular alterations, visual acuity improved significantly after cataract surgery in all patients in this study, while none of the patients demonstrated clinical CME (M. Eleftheriadou et al., 2010).
3. Pathogenesis, pathophysiology The formation of CME is due to leakage of perifoveal capillaries, which if severe enough, leads to pooling in the outer layers of the central retina. Cystoid spaces are formed in the foveal area, in the outer plexiform layer and Henle’s layer while some fluid accumulates in the nerve fiber layer, inside thin-walled cysts (Gass & Norton, 1966). Recently, histological findings have proved that the cysts may form also in the inner plexiform layer. The rod and cone photoreceptors in the area under the cysts are consistently found to be decreased in number.
Although the exact pathogenesis of post cataract CME is unknown, the main mechanism involved is considered to be inflammation. Inflammation in the vitreous, as described by Gass, represents a consistent finding in eyes with postoperative CME. This has been also documented in specimens of vitreous aspiration, where inflammatory cells were identified (Tso et al., 1982; Flach et al., 1998). In general, intraocular surgery seems to trigger the accumulation of macrophages and neutrophils that are further activated by circulating inflammatory agents, including cyclooxygenase and lipooxygenase metabolites, proteolytic agents and more, leading to the appearance of clinical signs of inflammation (perilimbal injection and anterior chamber flare). Cytokines such as interferon-γ, interleukin-2 and tumor necrosis factor-α also participate in the proccess inducing the production of cycloxygenase. (Wakefield & Lloyd, 1992; Miyake et al., 2000). Experimental studies of lens implantation in animal models have confirmed that trauma of the lens epithelial cells leads to the secretion of inflammatory mediators (Miyake et al., 1990). Other factors such as nitric oxide, complement and platelet-activating factor secreted by different cell types are believed to play important role in triggering inflammation postoperatively (Lightman & Chan, 1990).
The induced inflammation has been also suggested to affect the function of Bito’s pump, which is located in the ciliary epithelium and is responsible for the removal of inflammatory mediators from the eye (El-Harazi et al., 2001). Furthermore, the procedure of cataract surgery itself has been suggested recently to induce pro-inflammatory gene expression and protein secretion (Xu et al., 2011).